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Vecchio 22-07-2018, 01:17   #481
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Little research has been focused on the suppository (anal insertion) or pessary (vaginal insertion) methods of administration, also known as "plugging". These methods of administration are commonly carried out using an oral syringe. Heroin can be dissolved and withdrawn into an oral syringe which may then be lubricated and inserted into the anus or vagina before the plunger is pushed. The rectum or the vaginal canal is where the majority of the drug would likely be taken up, through the membranes lining their walls.
Vecchio 22-07-2018, 02:03   #482
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Confondere euforia con felicità è un grosso sbaglio
Vecchio 22-07-2018, 02:09   #483
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L'Abilify non mi convince mica.
Vecchio 22-07-2018, 02:15   #484
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Originariamente inviata da Shjatyzu Visualizza il messaggio
Latte, caffè, succo di frutta alla pera, e sertralina, sapore disgustoso, ma è una bevanda molto "frizzante".
La sertralina presa a parte o proprio sciolta nel miscuglio?
Vecchio 22-07-2018, 02:34   #485
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Disciolta
Prossima volta mettici pure della cioccolata e mi sa che sarà una bomba.
Vecchio 22-07-2018, 16:23   #486
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In Italia come siamo messi a reperibilita di questi farmaci? Negli Stati Uniti anche parecchie star ci sono rimaste secche com questa roba
Opioids: Why 'dangerous' drugs are still being used to treat pain http://www.bbc.co.uk/news/health-44797545
Vecchio 24-07-2018, 15:24   #487
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The atypical antipsychotics integrate with the serotonin (5-HT), norepinephrine (α, β), and dopamine (D) receptors in order to effectively treat schizophrenia.

D2 Receptor: Hyperactive dopaminergic activity on D2 receptors in the mesolimbic pathway is responsible for the positive symptoms of schizophrenia (hallucinations, delusions, paranoia). After taking an antipsychotic, antagonism of D2 receptors occurs throughout the entire brain, leading to a number of deleterious side effects from D2 receptor antagonism throughout the entire dopamine pathway system. Unfortunately, it’s not possible to affect D2 receptors only in the mesolimbic pathway.[58][Stahl AP Explained 1 - 1] Fortunately, 5-HT2A receptor antagonism reverses these side effects to some extent.[Stahl AP Explained 1 - 2] Reducing D2 dopaminergic activity in the mesolimbic pathway also results in an anhedonic effect, reducing pleasure, motivation, and the salience of one’s life experience. In the mesocortical pathway to the DLPFC and VMPFC, endogenous D2 receptor dopamine activity is sometimes low in schizophrenia, resulting in cognitive, affective, and, broadly, the negative symptoms of schizophrenia. D2 receptor antagonism here further compounds these problems. In the nigrostratial pathway, D2 receptor antagonism results in extrapyramidal symptoms. If this antagonism occurs long enough, symptoms of EPS may become permanent, even if antipsychotic use is discontinued. In the tuberoinfundibular pathway, D2 receptor antagonism results in elevated prolactin. If prolactin levels become high enough, hyperprolactinaemia may occur, resulting in sexual dysfunction, weight gain, more rapid demineralization of bones, and possibly galactorrhea and amenorrhea.[Stahl AP Explained 1 - 1]

5-HT2A Receptor: When serotonin is released on to postsynaptic 5-HT2A receptors, the dopamine neuron is inhibited, thus acting as a brake on dopamine release.[Stahl AP Explained 1 - 2] This brake is disrupted through action of a 5-HT2A antagonist, which cuts the brake cable, disinhibiting the dopamine neuron, and stimulating dopamine release. The result of this is that dopamine competes with antipsychotic D2 antagonistic action at D2 receptors, thereby reducing antagonistic binding there and eliminating or lowering D2 antagonistic effects in several pathways of the dopamine system.[Stahl AP Explained 1 - 2] In the nigrostratial pathway, it reduces EPS. In the tuberoinfundibular pathway, it reduces or eliminates prolactin elevation.[Stahl AP Explained 1 - 3] Dopamine release in the mesolimbic pathway from 5-HT2A antagonism does not appear to be as robust as in the other pathways of the dopamine system, thereby accounting for why atypical antipsychotics still retain part of their efficacy against the positive symptoms of schizophrenia through their D2 antagonism.[Stahl AP Explained 1 - 3] When 5-HT2A antagonistic agent particles occupy 5-HT2A receptors in the mesocortical pathway and in the prefrontal cortex, the negative symptoms of schizophrenia, affective symptoms, and cognitive deficits and abnormalities are treated and reduced.[Stahl AP Explained 1 - 3] Furthermore, 5-HT2A receptor antagonism blocks the serotonergic excitation of cortical pyramidal cells, reducing glutamate release, which in turn lowers hyperactive dopaminergic D2 receptor activity in the mesolimbic pathway, reducing or eliminating the positive symptoms of schizophrenia.[Stahl AP Explained 1 - 3][59][60]

Some effects of 5-HT1A receptor activation include decreased aggressive behavior/ideation,[61] increased sociability, and decreased anxiety and depression.[non-primary source needed] 5-HT2C activation blocks dopamine and inhibits norepinephrine release. Blockade of the 5-HT2C receptor increases serotonin, releasing norepinephrine and dopamine within the brain.[58] But neuronal reuptake of norepinephrine is limited sharply by some antipsychotics, for example ziprasidone. Increased norepinephrine can cause increased glucose levels, which is to say blood sugar levels.[62][63][64] Increased blood sugar levels by increased norepinephrine causes hunger in many humans, which is why weight gain occurs with some antipsychotics if the norepinephrine is not inhibited.[65][66][67][68][69] Inhibition of norepinephrine stabilizes mood in humans.[70] 5-HT6 receptor antagonists improve cognition, learning, and memory.[71] The 5-HT7 receptor is very potent for the mitigation of bipolar conditions and also yields an antidepressant effect. The antipsychotics asenapine,[72] lurasidone,[73][74] risperidone,[75] and aripiprazole[76] are very potent at the 5-HT7 receptor. Antagonistic affinity for the H1 receptor also has an antidepressant effect. H1 antagonism blocks serotonin and norepinephrine reuptake. Patients with increased histamine levels have been observed to have lower serotonin levels.[77] However, the H1 receptor is linked to weight gain. To have partial agonism at the 5-HT1A receptor can yield absence of weight gain in an antipsychotic. This is very relevant for ziprasidone,[78][79] but it creates a risk for a prolonged QTc interval.[80][81] On the other hand, blockade of the 5-HT3 receptor removes the risk for a prolonged QTc interval,[73] but then creates a larger risk for weight gain. Relation to the 5-HT3 receptor increases caloric uptake and glucose,[82] which is seen in clozapine and olanzapine.[83][84] Other ways for dopamine to resolve is to have agonism at both the D2 receptor and 5-HT1A receptor, which normalizes the dopamine level in the brain. This occurs with haloperidol and aripiprazole.

Whether the anhedonic, loss of pleasure and motivation effect resulting from dopamine insufficiency or blockade at D2 receptors in the mesolimbic pathway, which is mediated in some part by antipsychotics (and despite dopamine release in the mesocortical pathway from 5-HT2A antagonism, which is seen in atypical antipsychotics), or the positive mood, mood stabilization, and cognitive improvement effect resulting from atypical antipsychotic serotonergic activity is greater for the overall quality of life effect of an atypical antipsychotic is a question that is variable between individual experience and the atypical antipsychotic(s) being used.[58]
Come funzionano gli antipsicotici atipici.
Vecchio 25-07-2018, 00:01   #488
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Chissà che effetto fa la metanfetamina ai fobici.
Vecchio 25-07-2018, 00:43   #489
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Mi chiedo come mai la psichiatria non si riservi come trattamento estremo di casi di depressione resistenti a tutto l'utilizzo di metanfetamina, credo sia impossibile essere depressi con quella roba in corpo e i danni che fa in teoria son comunque minori del suicidio che è la distruzione totale del corpo.

Mi pare che l'anfetamina è usata in casi disperati di depressione ma la metanfetamina è davvero troppo potente e non la si usa anche perché poi è dipendenza garantita specie nella forma di cristalli che viene fumata.


La metanfetamina strabatte la cocaina come stimolante, credo sia lo stimolante più potente in natura, non fa dormire per giorni quindi pure la durata dell'effetto è superiore alla cocaina.
Vecchio 04-08-2018, 14:46   #490
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Ma qui si può postare oppure no?
Vecchio 21-08-2018, 09:05   #491
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Provate in passato almeno 5 su 6,onestamente non funzionano.
Vecchio 23-08-2018, 16:01   #492
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Si parla di usare l'LSD e l'MDMA in campo psichiatrico.
Vecchio 23-08-2018, 16:03   #493
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Si parla di usare l'LSD e l'MDMA in campo psichiatrico.


Ma l’hai visto lo spray a base di ketamina come terapia d’urto?
Vecchio 23-08-2018, 16:03   #494
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Ma l’hai visto lo spray a base di ketamina come terapia d’urto?
È già in commercio?
Vecchio 23-08-2018, 16:07   #495
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È già in commercio?


“Si tratta ancora di uno studio di fase 2 – quando la ricerca è ancora limitata a poche decine di pazienti e deve dimostrare la sicurezza e l’attività del farmaco – ma manca ancora la fase 3, estesa a migliaia di pazienti, che serve a confermare l’efficacia – prima che il farmaco possa essere approvato dalla Fda ed entrare poi in commercio. Gli autori, inoltre, si muovono con prudenza e avvisano la comunità scientifica che è necessario svolgere altre ricerche sul rischio di abuso e sulla dipendenza da ketamina, come sottolineano anche in un editoriale sulla stessa rivista.”

Ci vorranno anni se va bene..

Comunque le ricerche sul tema vanno solo nella direzione dell’uso di droghe alleggerite, altro che cure vere e proprie.
Vecchio 23-08-2018, 16:48   #496
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Follia pura
Vecchio 24-08-2018, 11:05   #497
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Fosse cosi facile chi ci andrebbe dagli psichiatri ecc
Vecchio 24-08-2018, 21:56   #498
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Alcohol & benzos - - - > ❤️
Vecchio 25-08-2018, 20:54   #499
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Due gocce e un goccio me li faccio va
Vecchio 28-08-2018, 20:08   #500
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Stasera devo dormire, prendiamo l’En ad alto dosaggio
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